OP0259 WHITE MATTER HYPERINTENSITY VOLUME IN UK BIOBANK PATIENTS WITH RHEUMATOID ARTHRITIS AND ULCERATIVE COLITIS
Authors: J. Cox, M. De Groot, J. Cole, S. Williams
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Rheumatoid arthritis (RA) and ulcerative colitis (UC) both result in higher levels of systemic inflammation and represent a significantly higher risk of cerebrovascular disease. The presence of this systemic inflammation has been linked to central nervous system effects and both diseases have increased rates of fatigue, brain fog and depression. Additionally, systemic inflammation has been implicated in decreasing the integrity of the blood brain barrier and potentially resulting in further involvement of the central nervous system in autoimmune diseases. <h3>Objectives</h3> The increased presence of white matter hyperintensities (WMH) has been proposed as a potential link to the central symptoms reported and the increased prevalence of cerebrovascular accidents in these diseases [1]. The present study aimed to analyse total volume of WMH in patients with RA and UC as compared to matched controls. <h3>Methods</h3> Data from 1,968 individuals in the UK Biobank Imaging sub-study were included in the present study [2]. This was divided into two separate patient populations with separate control groups matched to each in a 1:3 patient:control ratio. Data from 252 individuals (mean age ± SD =65.52 ± 7.03, 71.4% females) were included in the RA patient group with 756 age and sex matched controls (mean age ± SD = 65.52 ± 7.02, 71.4% females). Data from 240 individuals (mean age ± SD = 63.98 ± 7.06, 50.8% females) were included in the UC patient group with 720 age and sex matched controls (mean age ± SD = 63.98 ± 7.05, 50.8% females). This study utilised the total volume of WMH acquired using an automated segmentation approach called BIANCA and provided directly by the UKBiobank. Volumes were taken as a ratio of total brain volume and log transformed prior to a linear model regression being performed. Two separate models were run. One with age, sex, and ICV as covariates and a second model additionally including hypertension. <h3>Results</h3> We observed significantly larger total WMH volume in RA patients when compared to controls in model 1 (difference in WMH volume: 2286.0 mm<sup>3</sup>, SD ±84.5, p = 2.0e-08). The Cohen's effect size was <i>d</i> = 0.36 [95% CI 0.21, 0.5]. This effect was still substantial even with hypertension added as a covariate in model 2 (p = 3.7e-06). There was also a smaller, but still significant difference seen in UC patients compared to controls (difference in WMH volume: 237.1 mm<sup>3</sup>, SD ±82.1, p = 0.003). The Cohen's effect size was <i>d</i> = 0.19 [95% CI 0.04, 0.33]. As with the RA population hypertension is a strong contributing factor, however, the p value was still significant in model 2 (p = 0.03). <h3>Conclusion</h3> This is evidence that there is a cerebrovascular component to these diseases and that people with higher WMH burden may be at a higher risk of developing neurocognitive sequalae as part the disease. Further analysis of spatial mapping of WMH could provide further context for whether there are different patterns or distributions between RA and UC which could contribute to different central nervous system symptoms or cerebrovascular health risk factors. <h3>References</h3> [1]Dolapcioglu, C. and Dolapcioglu, H., (2015), 'Structural brain lesions in inflammatory bowel disease', World J Gastrointest Pathophysiol. vol. 6, no. 4, pp. 124 – 130 [2]Miller, K.L., Alfaro-Almagro, F., Bangerter, N.K. et al. (2016), 'Multimodal population brain imaging in the UK Biobank prospective epidemiological study', Nature Neuroscience, vol. 19, pp. 1523-1536. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> Jennifer Cox Grant/research support from: I am a GSK funded PhD student at King's College London, Employee of: I previously worked for GlaxoSmithKline, Marius de Groot Shareholder of: Dr. de Groot is a GSK employee with company shares, Employee of: Dr. de Groot is a current employee of GSK, James Cole: None declared, Steven Williams Consultant of: Dr. Williams has previously consulted for a number of pharmaceutical companies including GlaxoSmithKline, Johnson &amp; Johnson and Pfizer., Grant/research support from: Dr. Williams has received research funding from Bionomics, Eli Lilly, the Engineering and Physical Sciences Research Council, GlaxoSmithKline, Johnson &amp; Johnson, Lundbeck, the National Institute of Health Research, Pfizer, Takeda, and Wellcome Trust., Employee of: Dr. Williams previously worked for Pfizer.